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DNA Sequences Shaped by Selection for Stability

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  • Martin Ackermann
  • Lin Chao

Abstract

The sequence of a stretch of nucleotides affects its propensity for errors during replication and expression. Are proteins encoded by stable or unstable nucleotide sequences? If selection for variability is prevalent, one could expect an excess of unstable sequences. Alternatively, if selection against targets for errors were substantial, an excess of stable sequences would be expected. We screened the genome sequences of different organisms for an important determinant of stability, the presence of mononucleotide repeats. We find that codons are used to encode proteins in a way that avoids the emergence of mononucleotide repeats, and we can attribute this bias to selection rather than a neutral process. This indicates that selection for stability, rather than for the generation of variation, substantially influences how information is encoded in the genome. Synopsis: Mutations are a double-edged sword. Most mutations are deleterious to an organism's fitness. On the other hand, without mutation, evolutionary change cannot occur. The rate of mutation is partially controlled by the organism, and one determinant of the mutation rate is the DNA sequence itself. Some DNA sequences are prone to mutations and errors during gene expression, whereas other sequences are more stable. Do organisms typically use stable or unstable DNA sequences in their genes? Both possibilities might seem plausible, and both have been postulated. To answer this question, the authors studied whether organisms' DNA sequences are more or less stable than expected by chance. Analyzing the genomes of a bacterium, a yeast, and a nematode, they find a overwhelming prevalence of stable DNA sequences, suggesting that selection for genetic stability is more important than selection for the generation of variation.

Suggested Citation

  • Martin Ackermann & Lin Chao, 2006. "DNA Sequences Shaped by Selection for Stability," PLOS Genetics, Public Library of Science, vol. 2(2), pages 1-7, February.
  • Handle: RePEc:plo:pgen00:0020022
    DOI: 10.1371/journal.pgen.0020022
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